Recombinant Human BID Protein (PKSH033417)
For research use only.
| Synonyms | BH3-Interacting Domain Death Agonist, BID, p22 BID |
| Species | Human |
| Expression Host | E.coli |
| Sequence | Met 1-Asp195 |
| Accession | P55957 |
| Calculated Molecular Weight | 22.0 kDa |
| Observed Molecular Weight | 20 kDa |
| Tag | None |
| Bio-activity | Not validated for activity |
| Purity | > 95 % as determined by reducing SDS-PAGE. |
| Endotoxin | < 1.0 EU per μg of the protein as determined by the LAL method. |
| Storage | Store at < -20°C, stable for 6 months. Please minimize freeze-thaw cycles. |
| Shipping | This product is provided as liquid. It is shipped at frozen temperature with blue ice/gel packs. Upon receipt, store it immediately at < - 20°C. |
| Formulation | Supplied as a 0.2 μm filtered solution of 20mM PB, 100mM KCl, pH 7.4. |
| Reconstitution | Not Applicable |
| Background | BH3-Interacting Domain Death Agonist (BID) is a member of the Bcl-2 protein family which regulates outer mitochondrial membrane permeability. BID is a pro-apoptotic member that causes cytochrome c to be released from the mitochondria intermembrane space into the cytosol. BID contains only the BH3 domain; which is required for its interaction with the Bcl-2 family proteins and for its pro-death activity. BID is susceptible to proteolytic cleavage by caspases; calpains; Granzyme B and cathepsins. It is an integrating key regulator of the intrinsic death pathway that amplifies caspase-dependent and caspase-independent execution of neuronal apoptosis. Therefore pharmacological inhibition of BID provides a promising therapeutic strategy in neurological diseases where programmed cell death is prominent; and also offer a new strategy for the treatment of acute renal failure associated with ischemia-reperfusion. BID receives direct inputs from a key regulator of the cell cycle arrest/DNA repair machinery (ATM); and therefore is an excellent candidate to coordinate genotoxic stress responses and apoptotic cell death. BID is a novel pro-apoptosis Bcl-2 family protein that is activated by caspase 8 in response to Fas/TNF-R1 death receptor signals. Deletion of BID inhibits carcinogenesis in the liver; although this genetic alteration promotes tumorigenesis in the myeloid cells. This is likely related to the function of BID to promote cell cycle progression into S phase. BID could be also involved in the maintenance of genomic stability by engaging at mitosis checkpoint. |
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